Both male Zucker Fatty (mZF) and lower fat fed female Zucker Diabetic Fatty (LF-fZDF) rats are obese but remain normoglycemic. Male ZDF (mZDF) and high fat fed female ZDF rats (HF-fZDF) are also obese, but develop diabetes between 7 and 10 weeks of age. Although these models have been well studied, the mechanisms governing the adaptations to obesity in the normoglycemic animals, and the failure of adaptation in the animals that develop diabetes, remain unclear. Here we use quantitative morphometry and our recently developed IG model to elucidate the dynamics of insulin sensitivity (SI), beta cell secretory capacity (sc) and beta cell mass (m) in these four animal models. Both groups that remained normoglycemic with increasing obesity (mZF, LF-fZDF) exhibited increased m and constant sc in response to a falling SI. In rats that developed hyperglycemia (mZDF, HF-fZDF), there was a greater reduction in SI and slower expansion of m, with constant sc. sc decreased after glucose levels rose above 20 mM. Taken together these data suggest that excessive insulin resistance and insufficient beta cell mass adaptation play a primary role in the pathogenesis of diabetes.